Talk by Chris Moore of MIT on June 1, 2009. Given to the Redwood Center for Theoretical Neuroscience at UC Berkeley.
Our laboratory studies how rapid changes in neural organization, on the time scale of milliseconds to seconds, shape perception. Our key model system is the primary somatosensory cortex (SI), with a strong emphasis on the vibrissa 'barrel' cortex. In human MEG studies of tactile detection, we have shown that dynamics in the SI evoked response predict detection (Jones et al., 2007). This seminar will focus on two mechanisms for regulating such dynamics. First, we will discuss our recent studies of the origins of the gamma rhythm in the neocortex, a rhythm believed crucial to a variety of cognitive abilities including selective attention. To test the hypothesis that synchrony of fast-spiking inhibitory interneurons (FS) is causal in gamma genesis, we employed cell-type specific transfection of mouse neocortex with Channelrhodopsin-2. We found that selective optical drive of FS induced the gamma rhythm, while selective drive of excitatory cells induced lower frequency rhythms, a cell type specific double-dissociation in state induction. We further showed that phase of the gamma rhythm regulates the whisker-driven SI evoked response on the time scale milliseconds (Cardin et al., 2009). Second, we will discuss a less conventional mechanism for regulating cortical dynamics, the 'Hemo-Neural' hypothesis (Moore and Cao, 2008). This hypothesis predicts that local changes in hemodynamics--such as the functional hyperemia underlying the BOLD fMRI signal--can modulate local neural excitability . I will describe new methods we have developed for the selective control of blood flow in the brain to test this hypothesis, and our preliminary data showing cell-type specific modulation of SI evoked responses associated with local arterial dilation.